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Researchers from Tel Aviv University have discovered the molecular mechanism that regulates memory coding in brain cells

The group of researchers, led by Dr. Ina Slutsky from the Faculty of Medicine at Tel Aviv University in collaboration with the team of Prof. Paul Schlesinger from the Salk Institute in California, were able to observe the activity of neurons in a single synapse and understand why there is variation in the level of synapse activity, variation that is important for memory encoding at the cellular level. The results of the study show that the difference between the neural connections is caused by GABA, the molecule produced by neurons that inhibits their activity.

Dr. Ina Slutsky and Tal Laviv. Photo: Michal Kidron, Tel Aviv University
Dr. Ina Slutsky and Tal Laviv. Photo: Michal Kidron, Tel Aviv University
How does our brain encode memories? The basic units for creating memories are the synapses, which form the junction of information transfer from one nerve cell to another in the brain. The variation in the activity of synapses is a necessary feature in learning and memory processes in the brain. Previous studies have shown that some synapses are "quiet" and do not release neurotransmitter and therefore do not transmit information in a resting state, some transmit information constantly, and most of them are activated with variable probability. Although the resting state of synapses is a critical condition for memory encoding and processing, until now the molecular mechanism that causes variation in neurotransmitter release was not clear.

A new study, led by Dr. Ina Slutsky from the Faculty of Medicine, Tel Aviv University, which was published today in the prestigious journal Neuron, reveals the mechanism responsible for controlling the activity of individual synapses in neuronal networks.

The research was led by research student Tal Laviv and postdoctoral student Inbal Rivan. The researchers concentrated on studying synaptic activity in the hippocampus, an area of ​​the brain involved in the memory and learning process. They monitored the effect of the neurotransmitter GABA, a molecule common throughout the brain, which often inhibits neural activity. In the study it was found that the mechanism that regulates the difference between the synapses is carried out by the GABA molecule while activating GABAB receptors, which are found in the synapses and regulate the activity of the individual synapses locally. This study found how the release regulation mechanism works at the level of different synapses, while previous studies in the field investigated these phenomena only at the level of the cells and at the level of the entire tissue.

According to Dr. Slutsky, the success of the research was not guaranteed without a breakthrough in imaging methods that has occurred in recent years. "We were able to combine two high-resolution optical methods, one allows to see the activity of individual synapses and the other - dynamics of interactions between proteins at a level of up to 10 nanometers in a single synapse."

"We used the GABAB receptor proteins that were combined in the process of genetic engineering into luminous molecules in Prof. Schlesinger's laboratory at the Salk Institute. These engineered proteins made it possible to track their location and activity in neurons and constituted the detector for the level of GABAB receptor activity in a single synapse." Dr. Slutsky added.

Dr. Slutsky published an article in November 2009 dealing with amyloid beta - the protein whose excess causes cognitive decline in Alzheimer's patients, but her research revealed that it also has an important physiological role in the healthy brain - it regulates the transmission of signals between synapses. "Amyloid beta is a positive regulator, increasing the basal activity of synapses, while GABA is a negative regulator, decreasing their activity. These studies led us to the hypothesis that an increase in the basic activity of synapses is an initial and critical step in the development of a decline in learning and memory in neurodegenerative diseases," concludes Dr. Slutsky.

12 תגובות

  1. All I have to do is pick up GABA and say that I didn't understand anything from the explanation here about how memory works. But, if you say the research was good, then great.

  2. The title is exaggerated.
    The following is what is found in the study - "In the study it was found that the mechanism that regulates the difference between the synapses is carried out by the GABA molecule while activating the GABAB receptors, which are in the synapses and regulate the activity of the individual synapses locally. This study found how the release regulation mechanism works at the level of different synapses.
    If there is real coding in the brain it is still not understood at all.

  3. Dov Arad:
    You are right and wrong in the same response.
    how is it possible?
    You are wrong in that you think that the researchers did not come up with the directions of research that you are talking about. These are trivial ideas that any Internet commenter can think of.
    You are wrong in your assessment that this is something that will work.
    Memory is not material. is an organization of matter.
    In addition, it is a different organization for different people.

  4. The fact that they attach glowing molecules to the GABAB receptor proteins, doesn't it affect the function of GABAB in any way?

  5. To 5:
    Let's start with an easier one, erasing memories. And this is for a purely medical purpose, for example, for PTSD sufferers erasing memories can be part of an effective treatment.

  6. These nice (and of course talented) people do not know that their discoveries promote a situation where it will be possible to manipulate the memory and not exactly on the path of negation as it sounds!
    For example, speeding up the ability to learn by copying the memory of a person who is successful in his field and replacing it with another person who has no experience in the field, thus duplicating a "good" memory for as many people as they want. This is for example if people are urgently needed, let's say in the field of space for a short period of time, so it is not worth investing time and money in them Or good surgeons and good doctors in times of war or epidemics, etc.!
    But after reading this article, I come to the conclusion that copying the memory alone will not be enough and it will be necessary to memorize the material in order to make it "yours" and also to match the activity in the brain that requires minimum activity.. Therefore copying the material will be used as an infrastructure that will be inserted in a state where the brain will be in a state of complete relaxation without external disturbances and then the memorization will use the infrastructure introduced in a manipulative way (this the researchers will have to find and I trust them in this matter) and thus the learning time may be shortened to a tenth of the time it would take in normal learning!
    Nice, keep promoting the implementation of my ideas, who knows, maybe I'll still use one of them!!

  7. Inbal Rivan, who together with Tal Laviv, led the research in question and is now a researcher at the Weizmann Institute in Rehovot. It's amazing to see how in her humble and genuine way she contributes her tremendous experience, her wisdom and her sincere love for research that knows no bounds to the world of science! Greetings to Elkanoni's little brother!

  8. Amazing! Tal Laviv is a genius and a brilliant researcher, it was clear that we would hear about him and more than that it is clear that this is not the last time. Tal, the world of science has been waiting for you!

  9. Well done! This isn't the first time this group has hit the headlines! It seems that the combination of a brilliant group head and excellent highly motivated students has a future for science in Israel, I hope to hear a lot more about this successful group!

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